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Exercise training results in depot-specific adaptations to adipose tissue mitochondrial function.
Amy E Mendham1,2, Steen Larsen3,4, Cindy George5
1Non-communicable Diseases Research Unit, South African Medical Research Council, Cape Town, South Africa. amy.mendham@uct.ac.za.
Scientific Reports
|March 4, 2020
Summary
Exercise training improved mitochondrial function in gluteal and abdominal fat depots, enhancing insulin sensitivity and altering body fat distribution in obese women. This highlights exercise benefits for metabolic health.
Area of Science:
- Metabolic Health and Exercise Physiology
- Mitochondrial Biology
- Adipose Tissue Metabolism
Background:
- Mitochondrial dysfunction in adipose tissue is linked to insulin resistance and obesity.
- Subcutaneous adipose tissue depots (gluteal and abdominal) exhibit distinct metabolic characteristics.
- Understanding depot-specific mitochondrial adaptations to exercise is crucial for metabolic disease management.
Purpose of the Study:
- To compare mitochondrial function in gluteal (gSAT) and abdominal subcutaneous adipose tissue (aSAT) at baseline and after exercise.
- To examine depot-specific associations between mitochondrial function, body fat distribution, and insulin sensitivity (SI).
- To investigate the effects of a 12-week exercise intervention on mitochondrial function and metabolic parameters in obese women.
Main Methods:
- Randomized controlled trial involving obese South African women (n=45).
- Intervention group (n=23) underwent 12 weeks of aerobic and resistance training.
- High-resolution respirometry, fluorometry, frequently sampled intravenous glucose tolerance tests, dual-energy X-ray absorptiometry, and MRI were used to assess mitochondrial function, insulin sensitivity, body composition, and ectopic fat.
Main Results:
- Baseline gSAT exhibited higher mitochondrial respiratory capacity and hydrogen peroxide (H2O2) production than aSAT.
- Higher gSAT respiration correlated with increased gynoid fat, while higher gSAT H2O2 and lower aSAT respiration were linked to reduced insulin sensitivity.
- Exercise training improved insulin sensitivity, reduced gynoid fat and H2O2 production, and increased aSAT mitochondrial respiration, correlating with decreased body fat and altered hepatic fat content.
Conclusions:
- Significant depot-specific differences exist in mitochondrial function between gSAT and aSAT, influencing insulin sensitivity and body fat distribution.
- Exercise training induces beneficial adaptations in mitochondrial function across both gSAT and aSAT depots, improving insulin sensitivity.
- Targeting mitochondrial function in specific adipose depots through exercise may be a viable strategy for managing metabolic dysfunction and insulin resistance.
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